One of the major causes of blindness in the world is corneal clouding and scarring from a variety of diseases. Damage, disease, and dystrophy at the level of corneal endothelium and it's basement membrane, Descemet's membrane, frequently results in metaplasia of the corneal endothelial cells into fibroblast-like cells which produce a markedly abnormal basement membrane (Descemet's membrane) with a large collagen component. This abnormal change in endothelium is common to a number of corneal disease processes and results in corneal edema with progressive corneal scarring which can lead to blindness. The objectives of this study are to determine the role of collagen synthesis in the function of normal corneal endothelial cells and in endothelial cells which have been experimentally stimulated to metaplasia. Rabbit corneal endothelial cells will be established in culture. Synthesized collagen will be labeled with radioactive precursors and purified from other proteins. Fractionization of collagen synthesized by the cultured endothelial cells will be performed using SDS-polyacrylamide electrophoresis and collagen type determined by cyanogen-bromide peptide mapping. Fibroblastic metaplasia of rabbit corneal endothelial cells will be induced experimentally by external freezing of central cornea, producing a retrocorneal fibrous membrane. These diseased cells will be studied by routine histopathology and electron microscopy. Collagen synthesis by these cells will be studied during the course of the production of the retrocorneal fibrous membrane and the added insight into the pathogenesis of these defects at the level of the corneal endothelium and Descemet's membrane will provide information leading to possible therapy of such insults.